Muons as local probes of three-body correlations in the mixed state of type-II superconductors.

The vortex glass state formed by magnetic flux lines in a type-II superconductor is shown to possess nontrivial three-body correlations. While such correlations are usually difficult to measure in glassy systems, the magnetic fields associated with the flux vortices allow us to probe these via muon-spin rotation measurements of the local field distribution. We show via numerical simulations and analytic calculations that these observations provide detailed microscopic insight into the local order of the vortex glass and more generally validate a theoretical framework for correlations in glassy systems.

Experimental investigation of the dynamics of a vibrating grid in superfluid 4He over a range of temperatures and pressures.

In an earlier paper [Nichol, Phys. Rev. E, 70, 056307 (2004)] some of the present authors presented the results of an experimental study of the dynamics of a stretched grid driven into vibration at or near its resonant frequency in isotopically pure superfluid 4He over a range of pressures at a very low temperature, where the density of normal fluid is negligible. In this paper we present the results of a similar study, based on a different grid, but now including the temperature range where the normal fluid density is no longer insignificant. The new grid is very similar to the old one except for a small difference in the character of its surface roughness. In many respects the results at low temperature are similar to those for the old grid. At low amplitudes the results are somewhat history dependent, but in essence there is no damping greater than that in vacuo. At a critical amplitude corresponding to a velocity of about 50 mms(-1) there is a sudden and large increase in damping, which can be attributed to the generation of new vortex lines. Strange shifts in the resonant frequency at intermediate amplitudes observed with the old grid are no longer seen, however they must therefore have been associated with the different surface roughness, or perhaps were due simply to some artifact of the old grid, the details of which we are currently unable to determine. With the new grid we have studied both the damping at low amplitudes due to excitations of the normal fluid, and the dependence of the supercritical damping on temperature. We present evidence that in helium at low amplitudes there may be some enhancement in the effective mass of the grid in addition to that associated with potential flow of the helium. In some circumstances small satellite resonances are seen near the main fundamental grid resonance, which are attributed to coupling to some other oscillatory system within the experimental cell.

Spontaneous symmetry-breaking vortex lattice transitions in pure niobium.

We report an extensive investigation of magnetic vortex lattice (VL) structures in single crystals of pure niobium with the magnetic field applied parallel to a fourfold symmetry axis, so as to induce frustration between the cubic crystal symmetry and hexagonal VL coordination expected in an isotropic situation. We observe new VL structures and phase transitions; all the VL phases observed (including those with an exactly square unit cell) spontaneously break some crystal symmetry. One phase even has the lowest possible symmetry of a two-dimensional Bravais lattice. This is quite unlike the situation in high-Tc or borocarbide superconductors, where VL structures orient along particular directions of high crystal symmetry. The causes of this behavior are discussed.

Coexistence and coupling of superconductivity and magnetism in thin film structures.

Superconducting and magnetic order are usually mutually exclusive, and are found to coexist in relatively few materials. We have obtained direct evidence for a spin-density wave (SDW) coexisting with bulk superconductivity in a ferromagnetic-superconducting trilayer. In the superconducting state the amplitude of the SDW is enhanced and modeling the data also suggests a pi/2 phase shift of one component of the SDW, implying a profound coupling of these two forms of order.

Direct observation of the flux-line vortex glass phase in a type II superconductor.

The order of the vortex state in La1.9Sr0.1CuO4 is probed using muon-spin rotation and small-angle neutron scattering. A transition from a Bragg glass to a vortex glass is observed, where the latter is composed of disordered vortex lines. In the vicinity of the transition the microscopic behavior reflects a delicate interplay of thermally induced and pinning-induced disorder.

Binding of sodium dodecyl sulfate to linear and star homopolymers of the nonionic poly(methoxyhexa(ethylene glycol) methacrylate) and the polycation poly(2-(dimethylamino)ethyl methacrylate): electromotive force, isothermal titration calorimetry, surface tension, and small-angle neutron scattering measurements.

We investigated the binding of sodium dodecyl sulfate (SDS) to various linear and star polymers of the nonionic methoxyhexa(ethylene glycol) methacrylate (PMHEGMA) and the ionic 2-(dimethylamino)ethyl methacrylate (PDMAEMA), the latter being a polycation at low pH. The dodecyl sulfate ion selective electrode (EMF), isothermal titration calorimetry (ITC), and surface tension (ST) were applied to gain detailed information about interactions. In all cases there is evidence of significant binding of SDS over an extensive SDS concentration range spanning from ca. 10(-6) to 0.1 mol dm(-3). At pH 3, the polymer PDMAEMA is a strong polycation and here the binding is dominated by electrostatic 1:1 charge neutralization with the anionic surfactant. At their natural pH of 8.6, PMHEGMA and PDMAEMA polymers are essentially nonionic and bind SDS in the form of polymer-bound aggregates in the concentration range of ca. 1 x 10(-3) to 3 x 10(-2) mol dm(-3). All the polymers also bind SDS to a lesser extent at concentrations below 1 x 10(-3) mol dm(-3) reaching as low as 10(-7) mol dm(-3). This low concentration binding process involves the polymer and nonassociated SDS monomers. As far as we are aware, this is the first example that such a low concentration noncooperative binding process could be observed in SDS/neutral polymer systems by EMF and ST. We also showed that the nonionic surfactant hexa(ethylene glycol) mono-n-dodecyl ether (C12EO6) and the cationic cetyltrimethylammonium bromide (C16TAB) interact with star PDMAEMA. We believe that the interaction of C12EO6 and CTAB is of similar noncooperative type as the first SDS binding process in the range from ca. 10(-5) to 0.3 x 10(-3) mol dm(-3). At the high concentration binding limit Csat of SDS, the above polymers become fully saturated with bound SDS micelles. We applied small angle neutron scattering (SANS) to determine the structure and aggregation numbers of the star polymer/bound SDS micelles and calculated the stoichiometry of such supramolecular complexes. The SANS data on PDMAEMA star polymers in the presence of C12EO6 showed only a limited monomer binding in contrast to linear PDMAEMA, which showed monomer C12EO6 binding at low concentrations but micellar aggregates at 6 x 10(-3) mol dm(-3).

Triangular to square flux lattice phase transition in YBa2Cu3O7.

We have used the technique of small-angle neutron scattering to observe magnetic flux lines directly in a YBa2Cu3O7 single crystal at fields higher than previously reported. For field directions close to perpendicular to the CuO2 planes, we find that the flux lattice structure changes smoothly from a distorted triangular coordination to nearly perfectly square as the magnetic induction approaches 11 T. The orientation of the square flux lattice is as expected from recent d-wave theories but is 45 degrees from that recently observed in La(1.83)Sr(0.17)CuO(4+delta).

Distribution of transport current in a type-II superconductor studied by small-angle neutron scattering.

We report small-angle neutron scattering measurements on the vortex lattice in a PbIn polycrystal in the presence of an applied current. Using the rocking curves as a probe of the distribution of current in the sample, we observe that vortex pinning is due to the surface roughness. This leads to a surface current that persists in the flux-flow region. We show the influence of surface treatments on the distribution of this current.

Sulindac inhibits colorectal tumour growth, but not prostaglandin synthesis in the rat.

We have determined the dose-response relationship between sulindac administration and inhibition of tumour growth in the rat. The effect of tumour-inhibiting doses of sulindac on the production of prostaglandin E in tumours and macroscopically normal colon was then examined. Growth of pre-existing tumours was significantly reduced following administration of sulindac at 0.1 (P=0.004), 1 (P=0.01), 3 (P<0.001) and 10 mg/kg b.d. (P=0.002) for 4 weeks. There was no significant difference in prostaglandin E synthesis between tumours from control rats and those treated with sulindac at either 3 or 10 mg/kg b.d. (P=0.09 and 0.4, respectively). Prostaglandin E synthesis was reduced by 33 and 32% in macroscopically normal tissue from these treatment groups. These data show that sulindac inhibits tumour growth at low doses and do not support a role for the inhibition of prostaglandin synthesis, by sulindac, in the inhibition of tumour growth.

Inhibition of colon cancer precursors in the rat by sulindac sulphone is not dependent on inhibition of prostaglandin synthesis.

The non-steroidal anti-inflammatory drug, sulindac, inhibits the growth of colorectal tumours in animal models of colon cancer and causes regression of polyps in patients with familial adenomatous polyposis. The mechanism by which sulindac exerts this inhibitory effect is not known, but it has been postulated to be via the inhibition of prostaglandin synthesis. However, two recent studies have indicated that sulindac sulphone, the non-prostaglandin inhibiting metabolite of sulindac, may be important in tumour inhibition. In the present study, we examined the effect of sulindac sulphone on the formation of aberrant crypt foci, the earliest identifiable lesions in the development of colorectal cancer, in the rat colon. We have previously shown that sulindac causes a dose dependent inhibition of aberrant crypt formation in this model. Aberrant crypt foci were induced with two oral doses of 1,2-dimethyl hydrazine at 25 mg/kg per dose. Treatment with sulindac sulphone at either 10 mg/kg b.d., or 20 mg/kg, b.d., was started on the day following administration of the first carcinogen dose and was continued for 3 weeks. Colons were then removed and examined for aberrant crypt foci. Colonic crypts were visualized by staining the unsectioned colon in 0.2% methylene blue solution. There was a significant reduction in the number of aberrant foci in rats treated with sulindac sulphone at 20 mg/kg, b.d. (ANOVA, P = 0.0054). The mechanism by which non-steroidal anti-inflammatory drugs inhibit formation of aberrant crypt foci is not clear; however, these data suggest that it is not due to the inhibition of prostaglandin synthesis.

Sulindac and indomethacin inhibit formation of aberrant crypt foci in the colons of dimethyl hydrazine treated rats.

Aberrant crypt foci are microscopic lesions found in the colons of rodents treated with carcinogens, and in patients with premalignant colorectal conditions. They consist of single or multiple abnormal crypts and show cellular changes ranging from dysplasia to microscopic adenomacarcinoma. It is thought that these lesions represent the initial stages of the adenomacarcinoma path that results in the development of colorectal neoplasia. We have examined the effect of sulindac and indomethacin on the formation of aberrant crypt foci in rats treated with dimethylhydrazine (DMH). Aberrant crypt foci were induced in male Sprague-Dawley rats with two oral doses of dimethyl hydrazine at 25 mg/kg per dose. Rats were randomized to receive sulindac at 3 mg/kg (n = 20) or 10 mg/kg (n = 18) b.d., indomethacin at 1 mg/kg per day (n = 18) or 2 mg/kg per day (n = 19) or control (n = 37). Drug treatment was started on the day following the first dose of carcinogen and continued for 3 weeks. Colons were fixed flat overnight in 10% formalin and stained with 0.2%. Methylene Blue solution before being studied. There was a significant reduction in the number of aberrant crypt foci in rats treated with 10 mg/kg b.d., sulindac (P = 0.001) and indomethacin at 2 mg/kg per day (P = 0.0002). Sulindac, at 3 mg/kg b.d., and indomethacin, at 1 mg/kg per day, did not have a statistically significant effect (P = 0.089 and P = 0.052, respectively). None of the drug treatments affected the relative frequency of single crypt vs multiple crypt foci. Previous studies have shown that sulindac and indomethacin will significantly inhibit the growth and development of tumours in DMH treated rats. The current data suggest that one of the pathways of action of NSAID is to inhibit the formation of early preneoplastic lesions.

Immunohistochemical localisation of the c-fos oncoprotein in pancreatic cancers.

The c-fos gene product is a 55 kd nuclear protein bound to a cellular protein, p39. Expression of the c-fos oncogene is complex in that increased expression occurs in cultured cells during undifferentiated growth but decreased during terminal differentiation. We studied c-fos gene expression by streptavidin-biotin-peroxidase immunohistochemistry in pancreatic adenocarcinoma (N = 20), chronic pancreatitis (N = 9) and normal pancreas (N = 5). One islet cell tumour was included in the study. There was positive staining for c-fos oncoprotein in 15 of the 20 (75%) adenocarcinomas examined (9/12 moderate to poorly differentiated, 6/8 poorly differentiated). The single islet cell tumour investigated was also positive. Only 2 of 9 (22%) cases of chronic pancreatitis and 2 of 5 (40%) normal pancreata were positive. Stromal immunoreactivity was noted in all cancer cases while 5 of 9 (56%) chronic pancreatitis and 3 of 5 (60%) normal pancreas cases showed such staining. In conclusion, c-fos oncoprotein overexpression occurs more frequently in pancreatic cancers compared to chronic pancreatitis and normal pancreas. These findings are consistent with in vitro cell line studies of other cancers which showed increased expression of c-fos during undifferentiated growth.

p53 expression in laryngeal carcinoma.

The expression of the nuclear phosphoprotein, p53, was studied in 21 cases of squamous cell carcinoma of the larynx and 16 benign laryngeal lesions using the polyclonal rabbit antibody, CM1 (Novocastra Laboratories Ltd). Fourteen of the carcinomas showed nuclear staining whereas only one of the benign lesions exhibited presence of the protein. This suggests that, as with squamous cell carcinoma of the lung, p53 plays a role in the development of malignant disease of the larynx.

Immunohistochemical demonstration of the p53 tumour suppressor gene product in cancer of the pancreas and chronic pancreatitis.

The p53 tumour suppressor gene and its protein products after point mutations are currently attracting wide attention in the investigation of human tumours. In this study we present the findings on percutaneous pancreatic biopsies of 82 cases after routine processing and immunostaining for the polyclonal p53 antibody CM1, an antibody directed against both wild and mutant forms of p53 protein. There were 51 carcinomas, 5 islet cell tumours, 16 cases of chronic pancreatitis (including one with atypical ductal epithelium) and seven histologically normal pancreatic biopsy specimens. None of the seven normal cases showed any definite nuclear immunostaining for p53. Thirty-two (63%) of the pancreatic adenocarcinomas showed moderate to intense immunoreactivity. Of the 16 cases of chronic pancreatitis, 11 were negative and three showed equivocal immunostaining. The one case with ductal epithelial atypia showed mild to moderate immunoreactivity. All islet cell tumours were negative. The expression of the p53 gene, therefore, appears increased in the majority of pancreatic adenocarcinomas while this is not observed in chronic pancreatitis or normal pancreatic tissue. Nuclear immunoreactivity for p53 protein may represent mutant forms because of the short half-life of the wild-type protein. The lack of p53 expression in some cases of pancreatic adenocarcinoma may be due to different types of mutant proteins not detectable by the CM1 antibody. Nuclear immunoreactivity to the p53 protein in pancreatic biopsy is more suggestive of a malignant tumour than chronic pancreatitis.

A comparison between radioligand and immunohistochemical assay of hormone receptors in primary breast cancer.

The detection of oestrogen and progesterone receptor (ER and PgR) levels in human breast carcinoma has traditionally been performed using a biochemical radioligand binding method. This method has several disadvantages including the requirement for generous tissue samples, the production of radioactive waste products and the inability to exclude non-malignant cellular material from the assay process. An alternative method for detecting hormone receptors is available with the use of a monoclonal antibody specific for the ER or PgR receptor using immunocytochemical assay (ER-ICA or PgR-ICA). Although designed for use on frozen section material, with modifications this method can be used on paraffin sections of routinely fixed and processed tissue, on archival material and on very small specimens. Further, an objective assessment or scoring of staining intensity is possible using computerized video-image analysis. Forty-three cases of primary breast carcinoma, treated from 1989 to 1991 at Goulburn Valley Base Hospital, Shepparton were assessed for ER and PgR content using both the radioligand method and immunohistochemistry with video-image analysis, and the results were compared. Of the 43 cases, ER-ICA and ER had a concordance of 81% (P < 0.001, r = 0.58) and in 39 cases, PgR and PgR-ICA had a concordance of 87% (P < 0.001, r = 0.54). Because the sample for radioligand assay is of uncertain composition and the immunohistochemical stain can be scored specifically for malignant epithelium, a degree of discordance is thought to be mostly attributable to the limitations of the radioligand assay.